ライフサイエンスコーパス: synaptic strength

1 y as a novel therapeutic strategy to restore synaptic strength.

2 receptors that can be recruited to modulate synaptic strength.

3 osis (CME) is a key mechanism for regulating synaptic strength.

4 lso mediates the more elusive maintenance of synaptic strength.

5 tsynaptic density (PSD) determine excitatory synaptic strength.

6 hodiesterases (PDEs) potential regulators of synaptic strength.

7 e thought to result from specific changes in synaptic strength.

8 or density is a major variable in regulating synaptic strength.

9 t molecular mechanisms to maintain increased synaptic strength.

10 njunction with long-term depression (LTD) of synaptic strength.

11 synaptic plasticity that results in enhanced synaptic strength.

12 id receptors (AMPARs) in synapses determines synaptic strength.

13 iated with changes in gamma oscillations and synaptic strength.

14 short-term plasticity dynamically modulates synaptic strength.

15 ses is an important mechanism for regulating synaptic strength.

16 y synapses, where they maintain and modulate synaptic strength.

17 y that was largely responsible for increased synaptic strength.

18 roles for UNC-43/CaMKII in the regulation of synaptic strength.

19 correlated activity patterns into changes in synaptic strength.

20 s and transduce it to homeostatic changes in synaptic strength.

21 ic loss of surface AMPARs and downscaling of synaptic strength.

22 lization of rewarded STDP and hard limits on synaptic strength.

23 ipid-dependent control of C1-C2B to modulate synaptic strength.

24 ing recorded in vivo retrogradely influences synaptic strength.

25 s is thought to allow nonlinear summation of synaptic strength.

26 s, each form of plasticity directly modifies synaptic strength.

27 stimulated by Ca(2+)/CaM for enhancement of synaptic strength.

28 ic abundance and is implicated in modulating synaptic strength.

29 g APs brief, thus limiting Ca(2+) influx and synaptic strength.

30 aM-binding-impaired mutants even had reduced synaptic strength.

31 ) receptors act to nullify any net change in synaptic strength.

32 rodotoxin-induced scaling down of inhibitory synaptic strength.

33 GluA1 (also called Gria1) transcription and synaptic strength.

34 iation, triggered a long-lasting increase in synaptic strength.

35 synaptic scaffolds to proportionally reduce synaptic strength.

36 tant control mechanism for the regulation of synaptic strength.

37 ease rates, in turn, brings about changes in synaptic strength.

38 n important synaptic plasticity that weakens synaptic strength.

39 e constants, and reduced GlyR clustering and synaptic strength.

40 , and that conversion level is correlated to synaptic strength.

41 AMPA-type glutamate receptors in the PSD and synaptic strength.

42 he role of these vesicular SNAREs in setting synaptic strength.

43 t the postsynaptic density (PSD) to regulate synaptic strength.

44 input, enabling optical readout of relative synaptic strength.

45 to excitatory contacts had little effect on synaptic strength.

46 recordings from the IHCs to measure efferent synaptic strength.

47 ng activity-dependent plasticity to increase synaptic strength.

48 t is a presynaptic, long-lasting increase in synaptic strength.

49 rane AMPAR-associated protein that regulates synaptic strength.

50 TP induction but also for the maintenance of synaptic strength.

51 ability in population size, pulse timing and synaptic strength.

52 ization at synapses to regulate function and synaptic strength.

53 , such as receptors, can dramatically change synaptic strength.

54 t cell firing requires a critical inhibitory synaptic strength.

55 nism regulating such long-lasting changes in synaptic strength.

56 ade signaling plays a key role in regulating synaptic strength.

57 s important for the regulation of excitatory synaptic strength.

58 es for decades despite the short lifetime of synaptic strengths.

59 gnormally distributed, similar to reports of synaptic strengths.

60 reveal a rMS-induced reduction in GABAergic synaptic strength (2-4 h after stimulation), which is Ca

61 known to induce homeostatic upregulation of synaptic strength, a form of synaptic plasticity that di

62 is chronically suppressed, neurons increase synaptic strength across all affected synapses via synap

63 plicated in the modulation and regulation of synaptic strength, activity, maturation, and axonal rege

64 l cells typically show very small changes in synaptic strength after a pair of presynaptic and postsy

65 This proportional regulation of synaptic strength allows synaptic scaling to normalize a

66 On the other hand, changes in synaptic strength alone switched the regularity but not

67 A decreasing gradient of mossy fiber synaptic strength along the proximodistal axis is mirror

68 A similar activity-dependent reduction in synaptic strength also occurs in the developing brain an

69 Combined with the equalization of synaptic strength, an increase by CCh in the fraction of

70 NMDA receptors, which regulate synaptic strength and are implicated in learning and mem

71 Astrocytes can control basal synaptic strength and arteriole tone via their resting C

72 (AMPARs) are among the major determinants of synaptic strength and can be trafficked into and out of

73 embryonic spinal cord functions to maintain synaptic strength and challenge the view that scaling ac

74 e many forms of brain plasticity, changes in synaptic strength and changes in synapse number are part

75 ver, principles relating gamma oscillations, synaptic strength and circuit computations are unclear.

76 ns between them are important to controlling synaptic strength and circuit functions.

77 tem-specific functions such as modulation of synaptic strength and clearance of metabolites from the

78 Changes in synaptic strength and connectivity are thought to be a m

79 ation proposes a homeostatic increase in net synaptic strength and cortical excitability along with d

80 cell labeling, we identified an increase of synaptic strength and dendritic spine density specifical

81 necessary for long-lasting modifications in synaptic strength and dendritic spine dynamics that unde

82 tive drug use causes long-lasting changes in synaptic strength and dendritic spine morphology in the

83 lized translation in neurites helps regulate synaptic strength and development.

84 o acids in synaptic genes, directly altering synaptic strength and duration in response to environmen

85 Manipulating MEF2 alone alters synaptic strength and GluA1 content, but not synapse den

86 ypeptide 38 (PACAP38) alters hippocampal CA1 synaptic strength and GluA1 synaptic localization, its e

87 is characterized by compensatory changes in synaptic strength and intrinsic membrane properties in r

88 regulates the threshold for modification of synaptic strength and is an important regulator of learn

89 mGluR-LTD reduces synaptic strength and is relevant to learning and memory

90 or (NMDAR) stimulation causes a reduction in synaptic strength and is the central mechanism for long-

91 evented the injury-related loss of basal CA1 synaptic strength and key synaptic proteins and reduced

92 ic factor (BDNF), a key player in regulating synaptic strength and learning, is dysregulated followin

93 on synaptic proteins is a major regulator of synaptic strength and long-term plasticity, suggesting t

94 g mechanism for trans-synaptic regulation of synaptic strength and long-term plasticity.

95 On the other hand, basal synaptic strength and LTP were not affected in slices fr

96 olecular indices to non-invasively study net synaptic strength and LTP-like plasticity in humans afte

97 The basal changes in synaptic strength and morphology in cocaine-extinguished

98 ce for independent circadian oscillations in synaptic strength and morphology.

99 el mechanism by which noradrenaline controls synaptic strength and plasticity in the DRn.

100 smitter receptors is crucial for determining synaptic strength and plasticity, but the underlying mec

101 by clathrin-mediated endocytosis can control synaptic strength and plasticity.

102 role in postsynaptic protein scaffolding and synaptic strength and plasticity.

103 iverse ways by which HCN1 channels influence synaptic strength and plasticity.

104 synaptic densities and a potent regulator of synaptic strength and plasticity.

105 ic cocaine use is associated with changes in synaptic strength and resistance to the induction of syn

106 sleep, spontaneous activity renormalizes net synaptic strength and restores cellular homeostasis.

107 ty of neurotransmitter release, thus shaping synaptic strength and short-term synaptic plasticity.

108 ses and play an important role in regulating synaptic strength and stability.

109 Because evaluation of the determinants of synaptic strength and the extent of connectivity constit

110 ion in PE animals led to enhanced excitatory synaptic strength and the induction of CP-AMPAR-dependen

111 Basal synaptic strength and the maximal attainable t-LTP magni

112 cally adapt to external stimuli and regulate synaptic strength and ultimately network function.

113 follows sensory loss results from changes in synaptic strength and/or unmasking of subthreshold inter

114 works, including homeostatic effects on both synaptic strengths and firing rates.

115 gree of order in the spatial distribution of synaptic strengths and indicates that the relationship b

116 surface AMPARs, dendritic spine density, and synaptic strength, and also alters synaptic plasticity.

117 ion, the resulting enhancement in excitatory synaptic strength, and CP-AMPAR-dependent LTP are simila

118 Abeta-induced reductions in surface AMPARs, synaptic strength, and dendritic spine density.

119 r glutamate, AMPA receptors are critical for synaptic strength, and dysregulation of AMPA receptor-me

120 on depolarization resulted in a reduction of synaptic strength, and electrical stimulation of axons e

121 ich contributes to the calcium dependence of synaptic strength, and it influences the manner in which

122 luding regulation of synaptic communication, synaptic strength, and nerve regeneration.

123 o attenuated changes in dendrite morphology, synaptic strength, and NMDAR-dependent responses.

124 et-specific patterns of spatial convergence, synaptic strength, and receptor kinetics, resulting in d

125 fficking is a major mechanism for regulating synaptic strength, and that in vitro, trafficking of AMP

126 that synaptic Munc18-1 levels correlate with synaptic strength, and that synapses that recruit more M

127 Bidirectional changes of synaptic strength are crucial for the encoding of new me

128 nt bidirectional modifications of excitatory synaptic strength are essential for learning and storage

129 Surface AMPAR levels and synaptic strength are inversely regulated by Nedd4-1 and

130 Dynamic changes in synaptic strength are thought to be critical for higher

131 The possible effects of antidromic firing on synaptic strength are unknown.

132 tor learning and memory is developed whereby synaptic strengths are perpetually fluctuating without c

133 blocks homeostatic scaling up of inhibitory synaptic strength, as does knockdown of like-acetylgluco

134 ne self-administration, we found potentiated synaptic strength (assessed as the AMPA/NMDA current amp

135 movement (NREM) sleep, a global decrease in synaptic strength associated with slow waves (SWs) would

136 ecific and spine type-specific comparison of synaptic strength at a single spine level between cocain

137 Given that synaptic strength at CA3-CA1 synapses is related to the

138 Synaptic strength at excitatory synapses is determined b

139 The regulation of synaptic strength at gamma-aminobutyric acid (GABA)-ergi

140 uncaging and whole-cell recording to examine synaptic strength at individual spines on two distinct t

141 Susceptible mice exhibited increased synaptic strength at intralaminar thalamus (ILT), but no

142 silient animals displayed an upregulation of synaptic strength at large mushroom spines of D1-MSNs an

143 el is associated with transient increases in synaptic strength at prefrontal cortex synapses in the n

144 hat dopamine depletion selectively decreased synaptic strength at thalamic inputs to dMSNs, suggestin

145 urons reduces SEP amplitude but also reduces synaptic strength at the JON-GF synapse.

146 ential melastatin 8-mediated facilitation of synaptic strength at the level of the dorsal horn as an

147 How MAGUKs underlie synaptic strength at the molecular level is still not we

148 They mediate enhanced synaptic strength at the onset of burst-like activity, t

149 -timing-dependent plasticity (STDP) modifies synaptic strengths based on the relative timing of pre-

150 Long-term potentiation (LTP) of synaptic strength between hippocampal neurons is associa

151 the rat is sufficient to rapidly facilitate synaptic strength between primary afferent C-fibers and

152 -state propagation determines the changes of synaptic strengths between neurons.

153 PI(3,5)P2 levels was sufficient to regulate synaptic strength bidirectionally, with enhanced synapti

154 process transcends the simple modulation of synaptic strength by also regulating the signaling and i

155 fferent endings, an effect known to increase synaptic strength by enhancing neurotransmitter release

156 udies have shown that PE enhances excitatory synaptic strength by facilitating an anti-Hebbian form o

157 ocampal brain slices significantly increased synaptic strength by increasing functional synapses.

158 , a form of Hebbian plasticity, both enhance synaptic strength by increasing the abundance of postsyn

159 brate kinesin-1 heavy chain (KIF5), modifies synaptic strength by mediating the rapid delivery, remov

160 that a plasma membrane ion channel controls synaptic strength by modulating vesicular neurotransmitt

161 ne, a key striatal neuromodulator, increases synaptic strength by promoting surface insertion and/or

162 3, the C. elegans homolog of CaMKII, control synaptic strength by regulating motor-driven AMPAR trans

163 t can be converted into long-term changes in synaptic strength by reward-linked neuromodulators.

164 ults showed that the persistent reduction of synaptic strength by transient application of 20 mum tat

165 Thus, synaptic strength can be modulated by extracellular sign

166 Alterations in synaptic strength can result from modulation of AMPA rec

167 synaptic plasticity, a compensatory form of synaptic strength change, has attracted attention as a c

168 y strong input, followed by the decrement in synaptic strength coinciding with the pruning of climbin

169 ynamics remarkably robust against changes in synaptic strength compared with the nonrectifying case.

170 NCE STATEMENT: Activity-dependent changes in synaptic strength constitute a basic mechanism for memor

171 hat there is a minimum of 26 distinguishable synaptic strengths, corresponding to storing 4.7 bits of

172 These coordinated changes in FS-->SP synaptic strength define an expression pathway modulatin

173 zation of AMPARs and reduces corticostriatal synaptic strength, dephosphorylates DARPP-32 and GluA1,

174 tatic mechanisms can be harnessed to restore synaptic strength despite C9orf72 pathogenesis.

175 overy from synaptic depression, and enhanced synaptic strength despite smaller action-potential-elici

176 urrents between neuron types can explain why synaptic strength does not predict firing reliability/in

177 ressing inhibitory synapses showed increased synaptic strength due to an increase in the release prob

178 ynapses is a major mechanism for controlling synaptic strength during homeostatic scaling in response

179 ction is a fundamental mechanism controlling synaptic strength during long-term potentiation/depressi

180 operties and trafficking events that control synaptic strength during NMDA receptor-dependent synapti

181 ptor activation, and contributes to adapting synaptic strength during plasticity and neuromodulation.

182 on at FSN-PC and PC-FSN synapses, equalizing synaptic strength during repetitive presynaptic firing w

183 is offset by a homoeostatic reduction in net synaptic strength during sleep.

184 me system (UPS), which is known to influence synaptic strength, dynamically regulates Tomo-1 protein

185 We derive an expression for the synaptic strength dynamics showing that, by mapping the

186 As a result, synaptic strength exceeds acceptable levels and damages

187 n accompanying loss of PI(3,5)P2 and reduced synaptic strength following increased PI(3,5)P2 levels.

188 d their roles in regulating quantal size and synaptic strength, generating synaptic plasticity, maint

189 Rapid frequency-dependent changes in synaptic strength have key roles in sensory adaptation,

190 Activity-dependent changes in synaptic strength have long been postulated as cellular

191 at spontaneous release functions to regulate synaptic strength homeostatically in vivo SIGNIFICANCE S

192 The DG ligand agrin increases GABAergic synaptic strength in a DG-dependent manner that mimics h

193 es of bath application, E2 acutely increased synaptic strength in all groups except OVXLT rats that d

194 long-term depression (DCS-LTD) of excitatory synaptic strength in both human and mouse neocortical sl

195 Changes in glutamatergic synaptic strength in brain are dependent on AMPA-type gl

196 gest that presynaptic beta-neurexins control synaptic strength in excitatory synapses by regulating p

197 Measurements of synaptic strength in intact animals confirmed that both

198 mulation of heart cells, and potentiation of synaptic strength in neurons.

199 Long-term potentiation (LTP) of synaptic strength in nociceptive pathways is a cellular

200 Augmentation of synaptic strength in nociceptive pathways represents a c

201 esults support the hypothesis that increased synaptic strength in olfactory input networks mediates o

202 luN2B-containing NMDARs regulates excitatory synaptic strength in PFC determining basal levels of dep

203 ptor (GLP-1R) activation augments excitatory synaptic strength in PVN corticotropin-releasing hormone

204 aptic currents, exhibits enhanced excitatory synaptic strength in pyramidal cells that is induced pos

205 In this study, CaMKII-induced enhancement of synaptic strength in rat hippocampal neurons required bo

206 and quantal size were unaltered, the reduced synaptic strength in the absence of Cplx1 is most likely

207 hat TNFalpha is a regulator of glutamatergic synaptic strength in the adult striatum in a manner dist

208 ates activity-dependent long-term changes of synaptic strength in the CNS.

209 mechanisms underlying persistent changes in synaptic strength in the hippocampus, specifically long-

210 t fast glutamatergic transmission, increases synaptic strength in the hippocampus.

211 rimarily by evoking changes in glutamatergic synaptic strength in the mesocorticolimbic dopamine circ

212 ated cocaine exposure in vivo does not alter synaptic strength in the mouse prefrontal cortex during

213 ansient increase in dendritic spine size and synaptic strength in the nucleus accumbens.

214 J and utilized several approaches to restore synaptic strength in this model.

215 ich could be mediated by enhanced excitatory synaptic strength in ventral tegmental area (VTA) dopami

216 and the maintenance of augmented excitatory synaptic strength in VTA DA neurons and increased addict

217 Increased excitatory synaptic strength in VTA DA neurons is a critical cellul

218 st that, in PE animals, increased excitatory synaptic strength in VTA DA neurons might be susceptible

219 lt in the maintenance of enhanced excitatory synaptic strength in VTA DA neurons, which in turn contr

220 ondeterministic neuronal spiking and dynamic synaptic strengths in a randomly connected network are s

221 nge through activity-dependent modulation of synaptic strength, in older animals may augment TBI-indu

222 ts neighbors) and Hebbian learning (in which synaptic strength, in this case divisive normalization,

223 ic plasticity to induce long-term changes in synaptic strength, including long-term potentiation (LTP

224 function of sleep is to renormalize overall synaptic strength increased by wake.

225 now demonstrate that glial cells can control synaptic strength independent of neuronal activity.

226 gly, we show that homeostatic downscaling of synaptic strength is accompanied by an increase and decr

227 torage, but how such proportional scaling of synaptic strength is accomplished at the biophysical lev

228 neuronal mechanism for adjusting excitatory synaptic strength is clathrin-mediated endocytosis of po

229 In a presynaptic nerve terminal, synaptic strength is determined by the pool of readily r

230 t has been known for more than 70 years that synaptic strength is dynamically regulated in a use-depe

231 mice, RIM1/2 protein levels are reduced and synaptic strength is impaired.

232 In sharp contrast, alteration of inhibitory synaptic strength is independent of postsynaptic activat

233 Residual synaptic strength is maintained in a third phase, the st

234 This enhanced synaptic strength is mediated by a long-lasting increase

235 Synaptic strength is modulated by multiple factors inclu

236 hereas the spaced 5-HT-dependent increase in synaptic strength is partially dependent on translation

237 ession (LTD) at synapses in the adult brain, synaptic strength is reduced in an experience-dependent

238 We propose a model in which synaptic strength is the product of a synapse-specific H

239 A primary mechanism for increasing synaptic strength is the trafficking of alpha-amino-3-hy

240 the postsynaptic density (PSD) that promotes synaptic strength, is phosphorylated on threonine-19 (T1

241 ulations show that increasing Koff decreases synaptic strength multiplicatively, by reducing the frac

242 at interact with these complexes to modulate synaptic strength, namely proteins regulating actin fila

243 uronal processes is key to the alteration of synaptic strength necessary for long-term potentiation,

244 ,' and showed that drug-induced decreases in synaptic strength occur rapidly (within 30 min) and requ

245 synaptic competition process is the relative synaptic strength of competing terminals whereby stronge

246 ast, toluene vapor exposure had no effect on synaptic strength of DA neurons that project to the medi

247 , revealed by Ca(2+) responses, reflects the synaptic strength of each competing nerve terminal and t

248 wn as synaptic scaling, maintains the global synaptic strength of individual neurons in response to s

249 Up-scaling increased the synaptic strength of respiratory motoneurons and acted t

250 R deletion in iMSNs causes a decrease in the synaptic strength of striatopallidal neurons, which in t

251 of docked vesicles in PSs may promote a high synaptic strength of these synapses.

252 not exhibit a significant overall change in synaptic strength on D1-MSNs or D2-MSNs, we observed a s

253 uingly, the CaMKII inhibitor tatCN21 reduces synaptic strength only at high concentrations necessary

254 ion, we found that leptin reduces excitatory synaptic strength onto both melanin-concentrating hormon

255 Leptin-induced weakening of synaptic strength onto dopamine cells may underlie its i

256 havior are causally linked to alterations of synaptic strength onto nucleus accumbens (NAc) medium sp

257 tional range through compensatory changes in synaptic strength or intrinsic cellular excitability.

258 cuculline-induced scaling down of excitatory synaptic strength or the tetrodotoxin-induced scaling do

259 ticity is inactive at stable states and that synaptic strength overshoots during recovery from visual

260 form new GABAergic synapses that have little synaptic strength plasticity.

261 e ability of L-655,708 to restore excitatory synaptic strength rapidly may underlie its ability to re

262 However, how Shank3 regulates synaptic strength remains unclear.

263 tentiation (LTP) is a persistent increase in synaptic strength required for many behavioral adaptatio

264 d that the massed 5-HT-dependent increase in synaptic strength requires translation elongation, but n

265 We show that synaptic strength scales with the number of connections

266 lus-specific long-term potentiation (LTP) of synaptic strength selectively at the GABAergic component

267 Thus, basal synaptic strength, short-term plasticity, and homeostasi

268 to promote their internalization and weaken synaptic strength, similar to what occurs in Nedd4-1's e

269 ator that can effect long-lasting changes in synaptic strength such as long-term potentiation (LTP),

270 ins that promote mature spine morphology and synaptic strength, such as excitatory glutamate receptor

271 This protein loss also caused an increase in synaptic strength, suggesting that spontaneous neurotran

272 ceptor expression, and structural markers of synaptic strength, suggesting these EB neurons undergo "

273 insic noise massively increases the range of synaptic strengths supporting gamma oscillations and gri

274 The steep calcium dependence of synaptic strength that has been observed at many synapse

275 zinc-sensitive signaling system, regulating synaptic strength that may be impaired in ASD.

276 tion of surface AMPARs and the scaling up of synaptic strength that occur in response to chronic acti

277 LTP, LTD, and homeostatic scaling alter synaptic strength through changes in postsynaptic AMPA-t

278 ly regulates long-term potentiation (LTP) of synaptic strength through inhibition of AMPA receptor tr

279 that memories are encoded by modification of synaptic strengths through cellular mechanisms such as l

280 We demonstrate indices of increased net synaptic strength (TMS intensity to elicit a predefined

281 ynaptic release collectively serve to reduce synaptic strength to levels that fall below the threshol

282 Homeostatic responses critically adjust synaptic strengths to maintain stability in neuronal net

283 sistent changes in excitatory and inhibitory synaptic strengths to the ventral tegmental area (VTA) d

284 noise, variation in excitatory or inhibitory synaptic strength tunes the amplitude and frequency of g

285 hes to study how ongoing activity influences synaptic strength, using voltage- and current-clamp reco

286 Astrocytes can modulate synaptic strength via Ca(2+)-stimulated release of vario

287 signaling may play a role in fine-tuning of synaptic strengths via presynaptically-expressed CB1 rec

288 Synaptic strength was decreased by CaMKIIalpha knockdown

289 Increased synaptic strength was not due to changes in voltage-gate

290 he SA, a compensatory increase in excitatory synaptic strength was not observed following partial dea

291 In animals treated with cocaine, average synaptic strength was reduced specifically at large mush

292 e in nervous system function is equilibrium: synaptic strengths wax and wane, neuronal firing rates a

293 ivation is rapidly translated into increased synaptic strength, we identify a second phase where this

294 Thus, selective changes in CA3-CA1 synaptic strength were dependent on both the behavior di

295 quire normal long-term potentiation (LTP) of synaptic strength, which in turn requires binding of the

296 c function of the NMDAR in the regulation of synaptic strength, which relies on glutamate binding but

297 le in determining receptor concentration and synaptic strength, with known links between changes in b

298 atal day (p)17] or CP (p22-p25), and FS-->SP synaptic strength within layer 4 was assessed using conf

299 iated by activity-dependent modifications of synaptic strength within neuronal circuits.

300 gulation is essential for the maintenance of synaptic strength within the physiological range.